Airway epithelial cells are known to play a key role in orchestrating specific inflammatory immune responses important in the pathogenesis of asthma. This research proposal seeks to define the role of a signal transduction protein, STAT-1, in promoting immune cell influx and retention in the airway and how this disturbance of the airway epithelial cells may be curcial to the perpetuation of bronchial hyper-reactivity in the chronic asthmatic process.